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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [RNA-Seq]

ABSTRACT: We characterized the effect of GSK-LSD1 treatment on gene expression for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg)

ORGANISM(S): Homo sapiens

PROVIDER: GSE121425 | GEO | 2019/01/23

REPOSITORIES: GEO

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [ChIP-Seq]

Project description:We characterized the changes in histone modifications as well as the localization of LSD1 and GFI1B for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg) treated with GSK-LSD1

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [ChIP-Seq]

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [RNA-Seq]

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-01-23 | GSE121426 | GEO

Human small intestinal organoids grown with a specific protocol to enrich for Paneth cells were treated with an inhbitor (GSK-LSD1) for the epigenetic modulator LSD1.

Project description:To assess the role of LSD1 in human intestinal epithelium, human small intestinal organoids were treated with an inhibitor for LSD1 (GSK-LSD1) and compared to untreated organoids. The organoids were grown with specific conditions where Paneth cells are present in the organoids as similar experiments in mice show that Paneth cells disappear upon GSK-LSD1 treatment. Similar to mouse intestinal organoids, Paneth cells dissappear upon GSK-LSD1 treatment. Furthermore, we used these gene set enrichment analysis on these microarray data to show that these human intestinal organoids have a similar phenotype as mice epithelium without LSD1.

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Systemic LSD1 inhibition prevents aberrant remodeling of metabolism in obesity

Project description:The transition from lean to obese states involves systemic metabolic remodeling that impacts insulin sensitivity, lipid partitioning, inflammation, and glycemic control. Here, we have taken a pharmacological approach to test the role of a nutrient-regulated chromatin modifier, lysine-specific demethylase (LSD1), in obesity-associated metabolic reprogramming. We show that systemic administration of an LSD1 inhibitor (GSK-LSD1) reduces food intake and body weight, ameliorates non-alcoholic fatty liver disease (NAFLD), and improves insulin sensitivity and glycemic control in mouse models of obesity. GSK-LSD1 has little effect on systemic metabolism of lean mice, suggesting LSD1 has a context-dependent role in promoting maladaptive changes in obesity. Analysis of insulin target tissues identified white adipose tissue as the major site of insulin sensitization by GSK-LSD1, where it reduces adipocyte inflammation and lipolysis. We demonstrate that GSK-LSD1 reverses NAFLD in a non-hepatocyte-autonomous manner, suggesting an indirect mechanism potentially via inhibition of adipocyte lipolysis and subsequent effects on lipid partitioning. Pair-feeding experiments further revealed that effects of GSK-LSD1 on hyperglycemia and NAFLD are not a consequence of reduced food intake and weight loss. These findings suggest that targeting LSD1 could be a strategy for treatment of obesity and its associated complications including type 2 diabetes and NAFLD.

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RNA-seq of small intestinal organoids treated with an inhibitor for the epigenetic modifier LSD1

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